ABSTRACT
Surgical sepsis induced by major trauma, burns and hemorrhage remains a main cause of death of the patients in intensive care units, and may result in both the widespread activation and dysfunction of the innate and adaptive responses in the host immune system. A large amount of information concerning the subsets of innate and adaptive immune cells in sepsis has implicated that these cells, including neutrophils, macrophages, dendritic cells, T lymphocytes, regulatory T cells, and natural killer cells, have significant effects on immunoreactivity during acute insults or sepsis through modulating multiple receptor expressions or cytokine release, in turn contributing to the development and outcome of sepsis. Therefore, a deeper insight into the mechanism of immune regulatory dysfunction in surgical sepsis is of great significance in helping assess the prognosis of sepsis and guide the treatment of its complications.
ABSTRACT
High mobility group box-1 protein (HMGB1), which is a nuclear protein, participates in chromatin architecture and transcriptional regulation. When released from cells, HMGB1 also plays a well-established role as a pro-inflammatory mediator during innate immune responses to injury. In the initial stage of injury, there is a release of large quantities of early pro-inflammatory mediators to initiate or perpetuate immune responses against pathogens, but this pro-inflammatory period is transient, and it is followed by a prolonged period of immune suppression. At present, several lines of evidences have suggested that HMGB1 is a late cytokine provoking delayed endotoxin morbidity, which may enhance the production of early proinflammatory mediators, and it can contribute potently to the activation of different immune cells and play a role in the development of host cell-mediated immunity. The biology of HMGB1 has been extensively studied as a pro-inflammatory cytokine of systemic inflammation, however, this review will attempt to provide a summary of the effects of HMGB1 on different immune cells and its regulatory mechanism in acute insults.